Acute exposure of rabbits to diphenyl diselenide: a toxicological evaluation

✍ Scribed by Marcos Raniel Straliotto; Gianni Mancini; Jade de Oliveira; Evelise Maria Nazari; Yara Maria Rauh Müller; Alcir Dafre; Susana Ortiz; Edson Luiz Silva; Marcelo Farina; Alexandra Latini; João Batista Teixeira Rocha; Andreza Fabro de Bem

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 837 KB
• Volume: 30
• Category: Article
• ISSN: 0260-437X
• DOI: 10.1002/jat.1560

✦ Synopsis

Abstract

The simple organoselenium compound diphenyl diselenide (PhSe)~2~ is a promising new pharmacological agent. However, few toxicological evaluations of this molecule have been reported. We evaluated the effects of acute administration of (PhSe)~2~ on toxicological parameters in rabbits. Adult New Zealand rabbits were exposed to (PhSe)~2~ (5–500 µmol kg^−1^, intraperitoneally) once a day for 5 days. Exposure to 500 µmol kg^−1^ caused 85% mortality. Exposure to 50 µmol kg^−1^ of (PhSe)~2~ increased the glutathione levels in the hippocampus, kidney, heart, muscle and blood, whereas lipoperoxidation (TBARS) decreased in the cerebellum and kidney after exposure to 5 µmol kg^−1^. The activity of glutathione peroxidase increased in the heart and muscle of rabbits treated with 50 µmol kg^−1^ of (PhSe)~2~ and glutathione reductase activity was reduced in the cerebellum, cerebral cortex and kidney. Treatment with (PhSe)~2~ reduced the activity of δ‐aminolevulinate dehydratase in the hippocampus and increased this activity in the heart, but did not alter the activity of complexes I and II of the respiratory chain in the liver and brain. Hepatic and renal biochemical and histological parameters were not modified by (PhSe)~2~ and apoptosis was not detected in these tissues; however, the hepatic cells tended to accumulate fat vacuoles. These results indicated that acute toxicology to (PhSe)~2~ in rabbit is dependent on the dose, which should motivate further experiments on the therapeutic properties of this compound. Copyright © 2010 John Wiley & Sons, Ltd.